Defibrillation shocks depressed the Ca2+-pumping function of cardiac sarcoplasmic reticulum by uncoupling ATP hydrolysis and Ca2+ transport, potentially underlying postshock myocardial dysfunction.
Do transthoracic shocks depress Ca2+ transport function of cardiac sarcoplasmic reticulum in rats?
Defibrillation shocks depress the Ca2+-pumping function of the cardiac sarcoplasmic reticulum, providing a potential mechanism for postshock myocardial dysfunction.
Presently, the only therapy for ventricular fibrillation is delivery of high-voltage shocks. Despite "successful defibrillation," patients may have poor cardiac contractility, the mechanisms of which are unknown. Intracellular Ca2+ handling by the sarcoplasmic reticulum (SR) plays a major role in contractility. We tested the hypothesis that defibrillation shocks interfere with Ca2+ transport function of cardiac SR. Rats anesthetized with pentobarbital sodium had bilateral electrodes implanted subcutaneously for transthoracic shocks. A series of 10 shocks, 10 s apart, at 0-250 V was delivered from a trapezoidal defibrilator. The hearts were rapidly removed, SR-enriched membrane vesicles were isolated, and ATP-dependent Ca2+ uptake and Ca(2+)-stimulated ATP hydrolysis were determined. There was a marked, shock-related decline in Ca2+ uptake, whereas adenosinetriphosphatase activity remained unaltered. The polypeptide compositions were similar in control and shocked SR. In Langendorff hearts, shocks also decreased contractility and slowed relaxation. These data indicate that shocks with current densities similar to defibrillation depress Ca(2+)-pumping function of cardiac SR because of uncoupling of ATP hydrolysis and Ca2+ transport. Shock-induced impairment of Ca2+ pump function may underlie postshock myocardial dysfunction.
Jones et al. (Thu,) conducted a other in Postshock myocardial dysfunction. Transthoracic shocks vs. Control was evaluated on ATP-dependent Ca2+ uptake and Ca(2+)-stimulated ATP hydrolysis. Defibrillation shocks depressed the Ca2+-pumping function of cardiac sarcoplasmic reticulum by uncoupling ATP hydrolysis and Ca2+ transport, potentially underlying postshock myocardial dysfunction.